Cardiac valve insufficiency is a pathology that generally leads to a surgical intervention for the replacement of the diseased native heart valve. In the field of heart valve surgery both biological and mechanical prostheses are known, the former being generally made from portions of biological tissue (for example bovine pericardium), the latter being made e.g. either of metal materials, polymeric materials or composite materials, possibly clad with a biocompatible coating (i.e. pyrolitic carbon).
In a large majority of cases, a diseased native heart valve is found to allow a blood regurgitation through the leaflets, whereby a fraction of the blood flow which is actively (i.e. by a positive action) displaced by the pulsating heart leaks through the diseased valve in a direction opposite to that normally intended for the passage of blood flow due to sub-optimal coaptation of the valve leaflets.
Taking a diseased native heart valve as example, it is known that when the mitral valve is regurgitating a progressive decrease in left ventricle afterload (due to low pressure backward blood flow) and volume overload (i.e. high preload due to the regurgitated blood volume) occurs. This results, i.a. in a variation of the enzymatic myocytes equipment and of the pattern of actine-myosine cross bridge.
In other words, the entire heart cycle is affected, because the left ventricle experiences a lower blood pressure when ejecting blood through the aortic valve during systole due to the blood leak through the diseased mitral valve.
Additionally, when admitting blood into the left ventricle (diastole) via the mitral valve from the pulmonary veins, the left ventricle experiences a higher than normal preload due to the additional volume of blood that had previously leaked through the diseased valve due to the regurgitation and that now flows back in.
When a diseased mitral valve is replaced, the left ventricle experiences a sudden increase in afterload and a simultaneous decrease in preload. The first effect is due to the replacement mitral valve (i.e. prosthetic) being designed not to allow any blood leak (regurgitation) therethrough, so that when ejecting blood through the aortic valve during systole, the left ventricle experiences a higher blood pressure than that experienced with the diseased mitral heart valve because no blood leak occurs through the prosthetic mitral valve.
The second effect is due to the substantial absence of the regurgitated blood volume in the left ventricle during diastole.
A preload/afterload mismatch therefore occurs, which may lead to a left ventricle failure. Additionally, myocardial oxygen needs may increase as a consequence of a higher energy demand.
This furthermore may result in an intractable cardiogenic shock. In this situation the recovery sometimes requires several days of inotropic support.